Dendritic stability in a model of adult-onset IGF-I deficiency

Department of Physiology and Pharmacology, Wake Forest University, Winston-Salem, North Carolina, United States
Growth Hormone & IGF Research (Impact Factor: 1.41). 11/2005; 15(5):337-48. DOI: 10.1016/j.ghir.2005.07.002
Source: PubMed


A significant decrease in plasma levels of insulin-like growth factor-I (IGF-I) is one of the most robust hallmarks of aging and may contribute to functional changes associated with senescence. This study examined the role of IGF-I in the maintenance of adult dendritic morphology.
We utilized a model of the aging-related decrease in plasma IGF-I to examine whether such a decrease, in itself, leads to dendritic changes in the cerebral cortex. The dw/dw rat, originally of the Lewis strain, suffers from a spontaneous mutation in which growth hormone (GH) production is severely decreased. Since GH is responsible for the production of circulating IGF-I by the liver, these animals are deficient in plasma IGF-I. Homozygous dw/dw rats were administered porcine GH to sustain IGF-I levels during development and then GH injections were stopped as adults in order to examine the effects of adult-onset GH and IGF-I deficiency. Animals sacrificed after two or eight weeks of GH and IGF-I deficiency were compared to age-matched dw/dw animals that received GH both developmentally and throughout adulthood (GH/IGF-I replete). The dendritic arbors of pyramidal neurons in cingulate cortex were labeled by intracellular injection and reconstructed in three dimensions.
Comparing GH/IGF-I replete and deficient dw/dw rats, we found no differences in the apical or basal arbors of either layer two or layer five pyramidal neurons.
These findings indicate that a decrease in plasma levels of IGF-I is not sufficient in itself to produce dendritic changes like those seen in aging animals.

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